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Related Experiment Video

Updated: Jun 5, 2026

In Vivo Two-photon Imaging of Megakaryocytes and Proplatelets in the Mouse Skull Bone Marrow

In Vivo Two-photon Imaging of Megakaryocytes and Proplatelets in the Mouse Skull Bone Marrow

Published on: July 28, 2021

The clock gene Per2 is required for normal platelet formation and function.

Yue Zhao¹, Ying Zhang, Shiming Wang

¹Center for Molecular Metabolism, Nanjing University of Science & Technology, Nanjing, China.

Thrombosis Research

|December 28, 2010

Summary

This summary is machine-generated.

The clock gene Per2 is crucial for platelet formation and function. Loss of Per2 impairs megakaryocyte apoptosis, leading to reduced platelet counts and compromised hemostasis.

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Area of Science:

Hematology
Molecular Biology
Chronobiology

Background:

Platelet formation involves megakaryocyte apoptosis, a regulated genetic process.
The Per2 clock gene influences cell cycle control and apoptosis.
Per2 gene function is potentially linked to platelet production and function.

Purpose of the Study:

To investigate the role of the Per2 gene in megakaryopoiesis and platelet formation.
To determine the impact of Per2 deficiency on platelet function and hemostasis.

Main Methods:

Comparative analysis of Per2-null and wild-type mice.
Assessment of hemostasis and thrombopoiesis parameters (e.g., bleeding time, platelet counts, proplatelet formation).
Gene expression analysis using quantitative RT-PCR.

Main Results:

Per2-null mice exhibited ~50% lower platelet counts and impaired platelet aggregation/secretion.
Megakaryocytes from Per2-null mice showed increased ploidy, reduced proplatelet formation, and impaired apoptosis.
Gene expression changes in Per2-null mice included increased Tpo and C-mpl, decreased P53, and increased Bcl-xl/Bcl-2.

Conclusions:

The Per2 clock gene is essential for regulating megakaryocyte apoptosis.
Per2 is required for normal platelet formation and function, impacting hemostasis.